期刊
JOURNAL OF IMMUNOLOGY
卷 167, 期 9, 页码 5429-5438出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.167.9.5429
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资金
- NIDA NIH HHS [DA12444] Funding Source: Medline
- NIMH NIH HHS [MH61224, MH62261, MH59468, P30 MH062261] Funding Source: Medline
One of the consequences of IIIV infection is damage to the CNS. To characterize the virologic, immunologic, and functional factors involved in HIV-induced CNS disease, we analyzed the viral loads and T cell infiltrates in the brains of SIV-infected rhesus monkeys whose CNS function (sensory evoked potential) was impaired. Following infection, CNS evoked potentials were abnormal, indicating early CNS disease. Upon autopsy at I I wk post-SIV inoculation, the brains of infected animals contained over 5-fold more CD8(+) T cells than did uninfected controls. In both infected and uninfected groups, these CD8+ T cells presented distinct levels of activation markers (CD11a and CD95) at different sites: brain > CSF > spleen = blood > lymph nodes. The CD8+ cells obtained from the brains of infected monkeys expressed mRNA for cytolytic and proinflammatory molecules, such as granzymes A and B, perforin, and IFN-gamma. Therefore, the neurological dysfunctions correlated with increased numbers of CD8(+) T cells of an activated phenotype in the brain, suggesting that virus-host interactions contributed to the related CNS functional defects.
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